Kang Wenfei, Wong Li Chin, Shi Song-Hai, Hébert Jean M
Departments of Neuroscience and Genetics, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
J Neurosci. 2009 Nov 18;29(46):14571-80. doi: 10.1523/JNEUROSCI.3844-09.2009.
During corticogenesis, the balance between the self-renewal of radial glial stem cells and the production of their descendent progenitor cells is essential in generating the correct size and cell composition of the neocortex. How the stem-to-progenitor cell transition is regulated is poorly understood. FGFs are commonly implicated in promoting proliferation of neural precursor cells, but it is unclear how they exert their effects on stem cells, progenitor cells, or both in vivo. Here, three FGF receptor genes are simultaneously deleted during cortical neurogenesis. In these mutants, radial glia are depleted due to an increased transition from an uncommitted state to a more differentiated one, initially causing an increase in progenitors, but ultimately resulting in a smaller cortex. The proliferation rate of progenitors themselves, however, is unchanged. These results indicate that FGFs normally repress the radial glia to progenitor cell transition during corticogenesis.
在皮质发生过程中，放射状胶质干细胞的自我更新与其后代祖细胞产生之间的平衡对于形成正确大小和细胞组成的新皮质至关重要。目前对干细胞向祖细胞转变的调控机制了解甚少。成纤维细胞生长因子（FGFs）通常被认为可促进神经前体细胞的增殖，但尚不清楚它们在体内如何对干细胞、祖细胞或两者发挥作用。在此，在皮质神经发生过程中同时删除了三个FGF受体基因。在这些突变体中，放射状胶质细胞减少，这是由于从未分化状态向更分化状态的转变增加所致，最初导致祖细胞增多，但最终导致皮质变小。然而，祖细胞自身的增殖速率并未改变。这些结果表明，FGFs在皮质发生过程中通常会抑制放射状胶质细胞向祖细胞的转变。
